| Project/Area Number |
10670133
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Niigata University |
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Principal Investigator |
NAWA Hiroyuki Brain Research Institute, Niigata University Professor, 脳研究所, 教授 (50183083)
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| Co-Investigator(Kenkyū-buntansha) |
SHIRAKAWA Osamu Kobe University, Associate Professor, Faculty of Medicine, 医学部, 助教授 (40243307)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | schizophrenia / neurotrophin / phencyclidine / BDNF / sytokine / postmortem brain / neurotrophic |
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| Research Abstract |
In schizophrenic patients, pathological abnormality has been often found in the corticolimbic regions including prefrontalcortex and cingulate cortex.. Based on the hypothesis that developmental impairments in the brain involves schizophreniaetiology, we have investigated contribution of neuronal differentiation factors, neurotrophins, to this disease, which playcrucial roles in brain development. We measured levels of the three neurotrophins, NGF, BDNF and NT-3 in the postmortem brains by using a sandwich immunoassay. BDNF levels were increased in the hippocampus and cingulate cortex, but not in the other areas nor NT-3 levels in all the regions. These changes in BDNF levels were seen in the off-drug patients, excluding influences of neuroleptic treatments on BDNF. In addition, we also examined the expression of neurotrophins in the mode lanimals for schizophrenia, to which phencyclidine (PCP) had been administered chronically. In agreement, BDNF levels were elevated in the cingulate cortex and entorhinal cortex but NT-3 levels were not altered. These results suggest that abnormal expression of BDNF in the corticolimbic system contributes to the etiology or pathology of this disease.
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